{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu CC"],"funding":["E-Da Hospital"],"pagination":["8690"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12428822"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(17)"],"pubmed_abstract":["The causal contributions of specific mitochondrial genes to common pain phenotypes remain unclear. We employed a multi-omics Mendelian randomization (SMR) approach, integrating QTL data (expression, methylation, protein) for mitochondrial genes with GWAS summary statistics for seven pain phenotypes. We identified 18 candidate genes with robust SMR associations across omics layers. However, strong colocalization evidence (PP.H4 > 0.7) was largely absent, pointing towards complex genetic architectures. A notable exception was a strong signal for a shared causal variant found at the methylation level for the MCL1 gene in hip pain (PP.H4 = 0.962), nominating it as a high-confidence candidate. Additionally, genetically predicted higher protein levels of Glycine amidinotransferase (GATM) showed "],"journal":["International journal of molecular sciences"],"pubmed_title":["Mitochondrial Gene Regulation and Pain Susceptibility: A Multi-Omics Causal Inference Study."],"pmcid":["PMC12428822"],"funding_grant_id":["EDAHS111043","NCKUEDA10914"],"pubmed_authors":["Liu CC"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial Gene Regulation and Pain Susceptibility: A Multi-Omics Causal Inference Study.","description":"The causal contributions of specific mitochondrial genes to common pain phenotypes remain unclear. We employed a multi-omics Mendelian randomization (SMR) approach, integrating QTL data (expression, methylation, protein) for mitochondrial genes with GWAS summary statistics for seven pain phenotypes. We identified 18 candidate genes with robust SMR associations across omics layers. However, strong colocalization evidence (PP.H4 > 0.7) was largely absent, pointing towards complex genetic architectures. A notable exception was a strong signal for a shared causal variant found at the methylation level for the MCL1 gene in hip pain (PP.H4 = 0.962), nominating it as a high-confidence candidate. Additionally, genetically predicted higher protein levels of Glycine amidinotransferase (GATM) showed ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-26T20:05:51.726Z","creation":"2026-05-26T03:06:22.104Z"},"accession":"S-EPMC12428822","cross_references":{"pubmed":["40943610"],"doi":["10.3390/ijms26178690"]}}